The Mechanism of K‐Induced Vasodilation of the Coronary Vascular Bed of the Dog
作者:
PAUL MURRAY,
HARVEY SPARKS,
期刊:
Circulation Research
(OVID Available online 1978)
卷期:
Volume 42,
issue 1
页码: 35-42
ISSN:0009-7330
年代: 1978
出版商: OVID
数据来源: OVID
摘要:
We tested a number of hypotheses concerning the mechanism of K+-induced vasodilation of the coronary vascular bed. Blood flow in the circumflex artery was measured in pentobarbital-anesthetized, open-chest dogs. Intracircumflex artery bolus injections of 40 μmol of isosmotic KCI produced decreases in coronary vascular resistance ranging from 34% to 48%, depending on the initial resistance of the vascular bed. K+ administration had no effect on heart rate and produced a 4 mm Hg decrease in mean arterial pressure. K+ injection caused a 0.2 vol% increase in coronary sinus O2content in a preparation in which left common coronary flow was held constant. The magnitude of K+-induced vasodilation was not significantly affected by the administration of propranolol, atropine, phentolamine, or lidocaine. K+-induced vasodilation was attenuated (50%) by ouabain plus lidocaine. Acerylcholineinduced vasodilation was not significantly diminished by ouabain plus lidocaine. We conclude that the mechanism of K+-induced vasodilation does not involve an increase in the metabolic activity of the heart or an interaction between K+ and tissue neural elements. Our data do support the hypothesis that K+-induced vasodilation is at least partly the result of an activation of the electrogenic Na+—K+- transport system of coronary smooth muscle.
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